Defect of CD2- and CD3-mediated activation pathways in T cells of atopic patients: role of interleukin 2.

In the present work we analyzed the proliferative response of T lymphocytes from 11 atopic patients stimulated in vitro via either the CD2 or the CD3 pathway of cell activation. In both cases we found a significant decrease of thymidine incorporation in cell DNA in comparison with T cells from normal donors. The mechanism of this impaired proliferative response was analyzed. Atopic patients' T cells were found to secrete low quantities of interleukin 2 (IL2) and to express low amounts of Tac antigen, measured as both a percentage of Tac-positive cells and a mean fluorescence intensity of Tac antigen per cell. Addition of recombinant IL2 to cultures completely restored both cell proliferative response and Tac antigen expression. This effect was specific of IL2 since addition of IL1 or IL4 did not significantly affect T cell proliferative response. We conclude that atopic patients' T lymphocytes have a defect in both CD2 and CD3 pathways of cell activation relying on impairment of IL2 production, without involving IL2 responsiveness or other lymphokine defects.